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Biomedical subjects

M M Scheinman

Publications and source records attributed to M M Scheinman.

At least 37 records · Page 2Linked to original sources
PubMed1999

Use of electroanatomic mapping to delineate transseptal atrial conduction in humans.

BACKGROUND: Interaction between wave fronts in the right and left atrium may be important for maintenance of atrial fibrillation, but little is known about electrophysiological properties and preferential routes of transseptal conduction. METHODS AND RESULTS: Eighteen patients (age 44+/-12 years) without structural heart disease underwent right atrial electroanatomic mapping during pacing from the distal coronary sinus (CS) or the posterior left atrium. During distal CS pacing, 9 patients demonstrated a single transseptal breakthrough near the CS os, 1 patient in the high right atrium near the presumed insertion of Bachmann's bundle and 1 patient near the fossa ovalis. The mean activation time from stimulus to CS os was 48+/-15 ms compared with 86+/-15 ms to Bachmann's bundle insertion (P<0.01) and 59+/-23 ms to the fossa ovalis (P=NS and P<0.01, respectively). During left atrial pacing, the earliest right atrial activation was near Bachmann's bundle in 5 and near the fossa ovalis in 4 patients. The activation time from stimulus to CS os was 70+/-15 ms compared with 47+/-16 ms to Bachmann's bundle (P<0.01) and 59+/-25 ms to the fossa ovalis (P=NS). Whereas the total septal activation time was not significantly different during CS pacing compared with left atrial pacing (41+/-16 versus 33+/-17 ms), the total right atrial activation time was longer during CS pacing (117+/-49 versus 79+/-15 ms; P<0.05). CONCLUSIONS: Three distinct sites of early right atrial activation may be demonstrated during left atrial pacing. These sites are in accord with anatomic muscle bundles and may have relevance for maintenance of atrial flutter or fibrillation.

Adult↗
PubMed1999

Right atrial flutter due to lower loop reentry: mechanism and anatomic substrates.

BACKGROUND: The mechanisms of an atrial flutter (AFL) that is more rapid and at times more irregular than typical AFL are unknown. METHODS AND RESULTS: Twenty-nine patients with AFL were studied. Atrial electrograms were recorded from a 20-pole catheter placed against the tricuspid annulus (TA), with its distal electrodes lateral to the isthmus between the TA and the eustachian ridge (ER), and from the His bundle and coronary sinus catheters. Atrial extrastimuli were delivered in the TA-ER isthmus during typical AFL. Episodes of a right atrial flutter rhythm that was different from typical AFL were induced in 3 patients and occurred spontaneously in 3 patients. This sustained AFL, designated as lower-loop reentry (LLR), involved the lower right atrium (RA), as manifested by early breakthrough in the lower RA, wave-front collision in the high lateral RA or septum, and conduction through the TA-ER isthmus. Linear ablation resulting in bidirectional conduction block in the TA-ER isthmus terminated spontaneous LLR in 3 patients and rendered LLR noninducible in all patients. The cycle length of LLR was shorter than that of typical AFL (217+/-32 versus 272+/-40 ms, P<0. 01). Alternating LLR and typical AFL in 1 patient resulted in cycle length oscillation. CONCLUSIONS: LLR is a subtype of right atrial flutter and depends on conduction through the TA-ER isthmus.

Adult↗
PubMed1999

Electrophysiologic effects of adenosine in patients with supraventricular tachycardia.

BACKGROUND: We correlated the electrophysiologic (EP) effects of adenosine with tachycardia mechanisms in patients with supraventricular tachycardias (SVT). METHODS AND RESULTS: Adenosine was administered to 229 patients with SVTs during EP study: atrioventricular (AV) reentry (AVRT; n=59), typical atrioventricular node reentry (AVNRT; n=82), atypical AVNRT (n=13), permanent junctional reciprocating tachycardia (PJRT; n=12), atrial tachycardia (AT; n=53), and inappropriate sinus tachycardia (IST; n=10). There was no difference in incidence of tachycardia termination at the AV node in AVRT (85%) versus AVNRT (86%) after adenosine, but patients with AVRT showed increases in the ventriculoatrial (VA) intervals (13%) compared with typical AVNRT (0%), P<0.005. Changes in atrial, AV, or VA intervals after adenosine did not predict the mode of termination of long R-P tachycardias. For patients with AT, there was no correlation with location of the atrial focus and adenosine response. AV block after adenosine was only observed in AT patients (27%) or IST (30%). Patients with IST showed atrial cycle length increases after adenosine (P<0.05) with little change in activation sequence. The incidence of atrial fibrillation after adenosine was higher for those with AVRT (15%) compared with typical AVNRT (0%) P<0.001, or atypical AVNRT (0%) but similar to those with AT (11%) and PJRT (17%). CONCLUSIONS: The EP response to adenosine proved of limited value to identify the location of AT or SVT mechanisms. Features favoring AT were the presence of AV block or marked shortening of atrial cycle length before tachycardia suppression. Atrial fibrillation was more common after adenosine in patients with AVRT, PJRT, or AT. Patients with IST showed increases in cycle length with little change in atrial activation sequence after adenosine.

Adenosine↗
PubMed1999

A nodoventricular fiber associated with dual AV nodal conduction, AV nodal reentrant tachycardia, and anterior location of the slow AV nodal pathway.

We present a case of a patient with a nodoventricular tract, associated with dual AV nodal conduction and AV nodal reentrant tachycardia, and an anteroseptal location of the slow AV nodal pathway. The remarkable feature of this case is the site of successful ablation, in the anteroseptum just anterior and superior to the His bundle, where both preexcitation and dual AV nodal physiology were abolished.

Adult↗
PubMed1999

Failure of right atrial premature beats to reset atriofascicular tachycardia.

A patient with a right atriofascicular (Mahaim) tachycardia was found to have inducible antidromic supraventricular tachycardia, but atrial premature beats from the right atrial free wall failed to reset the tachycardia. An interesting transition from AV nodal reentry tachycardia to Mahaim tachycardia is also presented.

Adult↗
PubMed1999

Dynamic changes in electrogram morphology at functional lines of block in reentrant circuits during ventricular tachycardia in the infarcted canine heart: a new method to localize reentrant circuits from electrogram features using adaptive template matching.

INTRODUCTION: Fractionated, low-amplitude or long-duration electrograms have limited specificity for locating reentrant circuits causing ventricular tachycardia (VT). In this study a new method is described, adaptive template matching (ATM), based on the quantification of beat-to-beat changes in electrograms, for locating functional reentrant circuits that are relatively stable and cause monomorphic VT. METHODS AND RESULTS: Monomorphic VTs were induced in 4-day-old infarcted canine hearts by programmed stimulation and reentrant circuits mapped in the epicardial border zone with a 196 or 312 bipolar electrode array. For ATM analysis, a template electrogram from each electrode, during an early cycle, was matched with all subsequent (input) electrograms at the same site by weighting the inputs of amplitude, duration, average baseline, and phase lag. The mean square error (MSE) between template and input was the criterion used to adapt the weights, and was also a measure of changes in electrogram shape that occur from cycle to cycle. The variance of each of the weighting parameters at all electrode sites were plotted on a representation of the electrode array, and the location of the functional lines of block bounding the central common pathway of reentrant circuits with figure-of-eight characteristics, overlaid on the ATM map. Peaks of high variance were found to be coincident with functional lines of block during all tachycardia episodes. CONCLUSION: Specific beat-to-beat changes in electrograms occur at functional lines of block in reentrant circuits that can be quantified by ATM analysis, suggesting that these regions might be located without activation mapping. The method might be useful to guide ablation catheter position.

Animals↗
PubMed1998

Location of diastolic potentials in reentrant circuits causing sustained ventricular tachycardia in the infarcted canine heart: relationship to predicted critical ablation sites.

BACKGROUND: The complete reentrant circuit for ablation of reentrant ventricular tachycardia (VT) in humans can rarely be localized by mapping. As a result, surrogate markers, such as diastolic electrical activity, subsequently confirmed by entrainment, have been used. However, ablation at those sites has had variable efficacy. The reasons for this variability are not clear. METHODS AND RESULTS: We correlated activation maps of reentrant circuits in the epicardial border zone of 4-day old infarcted dog hearts with the corresponding ECGs for 45 VTs to determine the regions of the reentrant circuits activated during diastole. In VTs with a figure-8 reentrant pattern, the center point of the central common pathway, the part of the circuit critical for the maintenance of reentry, was activated in early diastole in 32 of 35 VTs (91.4%), in late diastole in 1 (2.9%), and in systole in 2 (5.7%). Regions outside the circuit were rarely activated in diastole. In 10 VTs, the reentrant circuit was characterized by a single reentrant loop. In these circuits, no one region was predicted to be critical for maintenance of reentry, and a segment of the circuits was activated during diastole. However, regions peripheral to the circuit were also activated during diastole. CONCLUSIONS: The pattern of reentrant activation determines the specificity of diastolic activity for locating critical sites for ablation of VT.

Animals↗
PubMed1998

Usefulness of pindolol in neurocardiogenic syncope.

We prospectively studied the efficacy of pindolol, a beta-adrenergic blocker with intrinsic sympathomimetic activity (ISA), for the prevention of syncope recurrences in 31 patients with recurrent neurocardiogenic syncope. Pindolol proved to be an effective treatment, even in patients who had previously failed treatment with conventional beta blockers, suggesting a clinical benefit from addition of ISA to beta blockade in this setting.

Adolescent↗
PubMed1998

Acceleration of typical atrial flutter due to double-wave reentry induced by programmed electrical stimulation.

BACKGROUND: Acceleration of reentrant tachycardia induced by programmed electrical stimulation is a well-documented phenomenon, but the mechanisms remain poorly understood. METHODS AND RESULTS: Twelve patients with typical atrial flutter were studied. Activation sequence of the underlying reentrant circuit was recorded by multiple multipolar electrodes placed in the right atrium. In five patients, 27 episodes of atrial flutter acceleration were induced by single extrastimuli delivered in the isthmus between the tricuspid annulus and eustachian ridge (TA-ER isthmus) and one by rapid overdrive atrial pacing. Analyses of the activation sequences, intracardiac electrograms, and 12-lead surface ECG P-wave morphology indicated that the acceleration was caused by two successive activation wave fronts circulating in the same direction along the same reentrant circuit (double-wave reentry, DWR). DWR was induced only within a narrow range of coupling interval, from 2 to 45 ms beyond the effective refractory period, and was associated with unidirectional antidromic block of the paced impulse. Patients with DWR had a shorter effective refractory period (138.8+/-13.4 versus 163.8+/-12.2 ms, P<.015) and larger excitable gap (124.0+/-22.6 versus 83.2+/-13.2 ms, P<.009) compared with patients without inducible DWR. All of the DWR episodes were transient. Most (78.6%) terminated after one of the double wave fronts was blocked in the TA-ER isthmus. CONCLUSIONS: DWR is one of the mechanisms responsible for programmed electrical stimulation-induced atrial flutter acceleration in human subjects. Its induction requires a sufficient excitable gap and antidromic unidirectional block of the paced impulse in the TA-ER isthmus. In addition, the TA-ER isthmus is the usual site of DWR termination.

Adult↗
PubMed1998

Narrow complex tachycardia with VA block: diagnostic and therapeutic implications.

To review our experience with cases of narrow complex tachycardia with VA block, highlighting the difficulties in the differential diagnosis, and the therapeutic implications. Prior reports of patients with narrow complex tachycardia with VA block consist of isolated case reports. The differential diagnosis of this disorder includes: automatic junctional tachycardia, AV nodal reentry with final upper common pathway block, concealed nodofascicular (ventricular) pathway, and intra-Hissian reentry. Between June 1994 and January 1996, six patients with narrow complex tachycardia with episodes of ventriculoatrial block were referred for evaluation. All six patients underwent attempted radiofrequency ablation of the putative arrhythmic site. Three of six patients had evidence suggestive of a nodofascicular tract. Intermittent antegrade conduction over a left-sided nodofascicular tract was present in two patients and the diagnosis of a concealed nodofascicular was made in the third patient after ruling out other tachycardia mechanisms. Two patients had automatic junctional tachycardia, and one patient had atrioventricular nodal reentry with proximal common pathway block. Attempted ablation in the posterior and mid-septum was unsuccessful in patients with nodofascicular tachycardia. In contrast, those with atrioventricular nodal reentry and automatic junctional tachycardia readily responded to ablation. The presence of a nodofascicular tachycardia should be suspected if: (1) intermittent antegrade preexcitation is recorded, (2) the tachycardia can be initiated with a single atrial premature producing two ventricular complexes, and (3) a single ventricular extrastimulus initiates SVT without a retrograde His deflection. The presence of a nodofascicular pathway is common in patients with narrow complex tachycardia and VA block. Unlike AV nodal reentry and automatic junctional tachycardia, the response to ablation is poor.

Adolescent↗
PubMed1998

Electroanatomical mapping and ablation of the substrate supporting intraatrial reentrant tachycardia after palliation for complex congenital heart disease.

In patients with congenital heart disease who have undergone palliative surgical interventions postoperative arrhythmias frequently complicate the clinical course. Intraatrial reentrant tachycardias (IARTs) are one of the most common forms of postoperative arrhythmias in these patients and can lead to significant morbidity and even mortality. Drug therapy and/or antitachycardia pacing have been disappointing. Ablative therapy with radiofrequency energy offers a potential for cure for these patients but the conventional approach using multielectrode recordings and fluoroscopic guidance is technically difficult and provides limited success. Recent development of a novel nonfluoroscopic technology with electroanatomical mapping using the CARTO mapping/ablation system has shown promising results in defining the arrhythmia circuit, facilitating diagnosis, and guiding ablative therapy. Based on our preliminary experience, a systematic approach to postoperative IART using electroanatomical mapping is described. Further studies are needed to fully evaluate the impact of this new technology on the management and therapy of IART.

Adult↗
PubMed1998

Adverse effects of amiodarone.

Amiodarone was introduced 30 years ago as an antianginal agent and subsequently has been used as an antiarrhythmic agent. This drug was initially used for patients with malignant ventricular arrhythmias; however, currently it is being used broadly for rate and rhythm control in patients with atrial fibrillation. At first, amiodarone was primarily used by cardiologists and today it is used throughout the medical profession. Amiodarone therapy can potentially result in a wide range of adverse effects. The majority of these adverse effects are dose related and reversible. The following is a review of the adverse effects and drug interactions of amiodarone along with recommendations for identification and management of these adverse effects.

Amiodarone↗
PubMed1997

Mortality benefit of implantable cardioverter-defibrillator therapy in patients with persistent malignant ventricular arrhythmias despite amiodarone treatment.

Implantable cardioverter defibrillators (ICDs) are very effective in preventing sudden cardiac death. However, debate continues as to whether ICD implantation is superior to amiodarone in prolonging survival in patients with life-threatening ventricular arrhythmias. Of 442 consecutive patients treated with amiodarone, we identified 48 patients with symptomatic ventricular arrhythmias who met all of the following inclusion criteria: (1) had inducible sustained ventricular tachycardia at baseline electrophysiologic study, (2) had an oral amiodarone load of at least 10 g over 10 to 14 days, (3) remained inducible with a hemodynamically unstable ventricular arrhythmia at follow-up electrophysiologic study, and (4) were advised to continue amiodarone therapy and undergo ICD implantation. Patients who agreed to undergo ICD implantation (n = 28) had a lower ejection fraction (29 +/- 9% vs 40 +/- 12% p <0.005) and were younger (61.0 +/- 10 vs 69 +/- 7 years, p <0.01) than patients who refused device implantation (n = 20). Using a Cox proportional-hazards model, defibrillator therapy was the strongest independent predictor of improved survival in patients with an ejection fraction < or =40% (RR = 0.42; 95% confidence interval 0.22 to 0.79). Thus, patients with depressed ejection fraction and continued inducibility of sustained ventricular tachycardia despite oral amiodarone loading have a poor prognosis. In such patients, ICDs are associated with a 58% reduction in total cardiac mortality.

Aged↗
PubMed1997

Risk of thromboembolism in chronic atrial flutter.

Anticoagulant therapy is not conventionally used in the treatment of patients with atrial flutter. This recommendation has been based on sparse clinical experience, and recent preliminary reports suggest a significant risk of thromboembolism for these patients. A retrospective study was undertaken to assess the frequency of thromboembolic events as well as potential risk factors for these events in a cohort of patients with atrial flutter referred for radiofrequency ablation treatment. Eighty-six consecutive patients with a primary diagnosis of atrial flutter were evaluated. A history of embolic events was noted in 12 of 86 patients (14%) with atrial flutter, with an annual risk of approximately 3%. There were no differences in the prevalence of coronary artery disease, cardiomyopathy, valvular disease, or atrial fibrillation between the 2 groups of patients having an embolic event and those of patients without embolic events. Left ventricular function and left atrial size were also similar between the 2 groups. The only significant risk factor was hypertension (p < 0.05). However, in a regression model with other clinical variables (i.e., age, gender, left atrial size, presence or absence of any cardiac disease, length of time in flutter, left ventricular function, type of flutter, flutter cycle length, type of secondary arrhythmias) no significant predictors were found. Patients with transient ischemic attacks or pulmonary emboli were then excluded from the analysis in order to compare the thromboembolic risk in the present study to that reported in major atrial fibrillation trials. The overall risk becomes 7% (6 of 86), which over a mean follow-up period of 4.5 years yields an annual risk of approximately 1.6%. Although this risk is only 1/3 of that for patients with atrial fibrillation, this risk is higher than previously recognized for patients with chronic atrial flutter. Anticoagulant therapy should be seriously considered for these patients.

Adult↗
PubMed1997

Tachycardia-induced cardiomyopathy: a review of animal models and clinical studies.

The increasing prevalence of congestive heart failure has focused importance on the search for potentially reversible etiologies of cardiomyopathy. The concept that incessant or chronic tachycardias can lead to ventricular dysfunction that is reversible is supported by both animal models of chronic rapid pacing as well as human studies documenting improvement in ventricular function with tachycardia rate or rhythm control. Sustained rapid pacing in experimental animal models can produce severe biventricular systolic dysfunction. Hemodynamic changes occur as soon as 24 h after rapid pacing, with continued deterioration in ventricular function for up to 3 to 5 weeks, resulting in end-stage heart failure. The recovery from pacing-induced cardiomyopathy demonstrates that the myopathic process associated with rapid heart rates is largely reversible. Within 48 h after termination of pacing, hemodynamic variables approach control levels, and left ventricular ejection fraction shows significant recovery with subsequent normalization after 1 to 2 weeks. In humans, descriptions of reversal of cardiomyopathy with rate or rhythm control of incessant or chronic tachycardias have been reported with atrial tachycardias, accessory pathway reciprocating tachycardias, atrioventricular (AV) node reentry and atrial fibrillation (AF) with rapid ventricular responses. Control of AF rapid ventricular responses has been demonstrated to improve ventricular dysfunction with cardioversion to sinus rhythm, pharmacologic ventricular rate control and AV junction ablation and permanent ventricular pacing. The investigation of potential tachycardia-induced cardiomyopathy in patients with heart failure requires further prospective confirmation in larger numbers of patients, with study of mechanisms, patient groups affected and optimal therapies.

Animals↗
PubMed1997

Frequency of disabling symptoms in supraventricular tachycardia.

The purposes of this study were to describe: clinical symptoms in a sample of consecutive patients with supraventricular tachycardia (SVT); incidence of sudden death, syncope, and other disabling symptoms; whether these symptoms differ by tachycardia mechanism; and to identify predictor variables of syncope in patients with SVT. Data were collected from chart reviews of 167 consecutive patients with SVT admitted for radiofrequency ablation. Three patients (2%) had nonlethal cardiac arrest, and a total of 16% (26 of 183) received at least 1 external direct-current shock for arrhythmia management. Twenty percent of subjects (33 of 167) reported at least 1 episode of syncope which was preceded by palpitations. The most frequent symptoms were: palpitations (96%), dizziness (75%), and shortness of breath (47%). We found atrioventricular nodal reentrant tachycardia (AVNRT) in 64 patients, atrioventricular-reciprocating tachycardia (AVRT) in 59, atrial tachycardia in 22, and atrial flutter in 22. The symptom profiles of patients with AVNRT, AVRT, and atrial tachycardia were very similar, but differed significantly (p <0.05) from those reported in the atrial flutter group. Multivariate analysis showed that heart rate > or = 170 beats/min was the only independent risk factor for syncope. Chi-square analysis demonstrated that SVT patients with heart rate > or = 170 beats/min had significantly more dizziness and syncope. Thus, despite a low incidence of associated heart disease, and good left ventricular function, there was a high frequency of disabling, potentially life-threatening symptoms associated with episodes of SVT in this sample. SVT can have potentially lethal consequences, and is more disruptive than previously thought.

Adult↗